<B>thrombus,mural atrial </B>

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thrombus,mural atrial

Etiology:

• Only rare hypercoaguable states due to genetic deficiencies of anticoagulants (antithrombin III, protein C and protein S) are known specific causes.
• Multiple factors involved in the pathogenesis of most thromboses, including a probable state of hypercoaguability, due to causes unknown. In contrast to hypocoaguable states, there are no current objective quantitative measures of hypercoaguability available.

Pathogenesis:

• Endothelial injury: Thrombi on atheromatous plagues, overlying myocardial infarcts, valvular endocarditis, hemodynamic trauma due to high pressures, or stenosis of valves.
• Stasis: Leg DVT's begin in valve pockets where eddies persist in upright position and washed out by elevation of legs. Abetted by immobility. Atrial thrombi with mitral stenosis and /or AF.
• Hypercoaguable states: See Etiology. Metastatic cancers, smoking, obesity, advanced age, SLE.

Epidemiology:

• RE: Deep vein thrombosis (DVT) and pulmonary emboli (PE). Massive PE cause 50,000 deaths per year. Actual incidence much higher, with 60% of autopsies showing PE (1963), which are mostly asymptomatic. Incidence probably rising with increasing surgical interventions, advances in intensive care, and longevity.
• Epidemiology of other effects of thrombosis, i.e. arterial thrombi complicating atherosclerosis & mural thrombi, vary with associated syndrome.

General Gross Description:

• Venous: A dark red clot forming a cast, equivalent to clotted blood in a test tube, due to stasis. Postmortem clots are ruled out by gross features, lacking cast form, wall and valve impressions.
• Mural thrombi: Friable brown discrete adherent mounds with typical uniformly wrinkled surfaces, the lines of Zahn due to genesis in flowing blood. Occur in cardiac chambers, aorta, and iliacs.
• Arterial: Usually a completely occlusive, dark red clot. Postmortem clots are cord like and elastic.

General Microscopic Description:

• Venous: Sheets of red cells. Fibrin component not visible. Outer rims may show a few lines of Zahn.
• Mural thrombi: Classical lines of Zahn with even layers of ridges of platelets with adherent wbc's separated by valleys of red cells. This is proof of antemortem genesis because blood flow needed.
• Arterial: Mostly venous-like when due to injuries of atherosclerosis. But, meticulous study of total thrombus will reveal focus of endothelial injury with nidus of platelet and fibrin thrombus.

Clinical Correlations:

• Venous: May be asymptomatic or have leg edema and/or calf tenderness due to distension of veins. Pulmonary emboli may be asymptomatic or cause unexplained dyspnea and/or sudden death.
• Mural thrombi: Can embolize to brain, spleen, kidneys and limbs with asociated syndromes. Vegetations of endocarditis can also embolize to coronary arteries with myocardial infarction.
• Arterial: Common cause of acute syndromes of visceral infarction and gangrene of extremiries

References:
•1. Robbins Pathologic Basis of Disease. Cotran, RS, Kumar, V, Robbins, SL, and Schoen, FJ. 5th Edition 1994. pp. 105-112. •2. Harrison's Principles of Internal Medicine, 13th edition, 1994. pp.1214-1215. •3. Freiman, DG et al: Fr